Vagal Nerve Stimulation Protects Against Cerebral Ischemia-Reperfusion Injury in Rats by Inhibiting Autophagy and Apoptosis

Cumulative evidence suggests that neuronal death including autophagy, apoptosis, and necrosis is closely related to the occurrence and development of cerebral ischemia-reperfusion (I/R) injury. Moreover, vagal nerve stimulation (VNS) is involved in many different neuroprotective and neuroplasticity pathways. Thus, VNS may be a novel approach for treating various neurodegenerative diseases. The present study aims to determine whether VNS protects against cerebral I/R injury in rats by inhibiting autophagy and apoptosis. Cerebral I/R injury is induced by middle cerebral artery occlusion (MCAO) and VNS is carried out. Infarct volume, neurological deficit, autophagy, and apoptosis are examined 24 h after reperfusion. Vagal nerve stimulation decreases infarct volume and suppresses neurological deficit. Moreover, obvious autophagy and apoptosis are detected in rats that have undergone I/R, and VNS inhibits autophagy and apoptosis. Vagal nerve stimulation exerts neuroprotective effects following I/R injury by inhibiting autophagy and apoptosis.